Pramod Pulaamba
56 statements · 1 topic
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We know that hypotension in the context of, uh, closed head injury is a very poor, uh, prognosticator and therefore, we should at all costs, try to maintain blood pressure.
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Traumatic Brain Injury
Even for those with suspected spinal cord injury, it is, that is no longer considered, uh, um, um, Actually effective therapy and it actually may cause detriment.
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Traumatic Brain Injury
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Pramod's statements about Traumatic Brain Injury 56 statements
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Traumatic Brain Injury
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This is a, a, a pretty classic, uh, case, and considering that we've already have a CT scan and we've identified a small epidural, I think it's, it behooves us to immediately call our neurosurgical colleagues to ensure that this epidural bleed does not require surgical evacuation.
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For a patient with small epidural hematoma, immediate neurosurgical consultation is needed to determine if surgical evacuation is required.
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Small epidurals may be managed with repeat CT scan in several hours or clinical observation for deterioration rather than immediate surgery.
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ICP monitoring should be discussed with neurosurgeons for patients being managed for potential intracranial pressure issues.
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Invasive blood pressure monitoring is needed for accurate blood pressure identification in patients with intracranial hypertension.
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So remembering that cerebral perfusion pressure is your mean arterial pressure minus your intracranial pressure.
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Cerebral perfusion pressure equals mean arterial pressure minus intracranial pressure.
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Most guidelines suggest keeping cerebral perfusion pressure greater than 45 mmHg as minimal acceptable, sometimes 55 mmHg in children.
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Most, uh, guidelines suggest that keeping a CPP greater than 45 would be the minimal acceptable. Sometimes in children, this would be, uh, 55.
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Acute intracranial hypertension may first manifest as dilation of the ipsilateral pupil or progressive bradycardia with hypertension.
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Acute ICP management includes raising head of bed to improve venous drainage, providing oxygen, and bag valve masking.
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Opening an ICP drain is one of the first interventions to evacuate fluid and reduce pressure.
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3% normal saline at 5 mL per kilogram will generally increase serum sodium by 3 to 5 mEq per liter.
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The reason why I like 2% normal saline, uh, actually, there's, there are several reasons. One, it's easy to give. Two, it keeps your sodium a little bit higher, so, therefore, um, you actually will have some some, some long-lasting ability to reduce cerebral swelling. Three, it has a much higher osmolarity limit, uh, compared to Mannitol. Uh, it's 360 instead of 320 millimoles.
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3% normal saline has a higher osmolarity limit (360 millimoles) compared to Mannitol (320 millimoles).
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Hypotension in the context of closed head injury is a very poor prognosticator and should be avoided at all costs.
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Quotation
We know that hypotension in the context of, uh, closed head injury is a very poor, uh, prognosticator and therefore, we should at all costs, try to maintain blood pressure.
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In older children and teenagers, systolic blood pressure should be kept above 90 or 95 mmHg; younger children should use age-appropriate norms.
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Norepinephrine can be used to drive up blood pressure to maintain cerebral perfusion.
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With respect to Mannitol, there is actually no evidence to suggest that one is better than the other based on the most recent guidelines, uh, that were published in pediatric critical care medicine.
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Based on the most recent guidelines published in Pediatric Critical Care Medicine, there is no evidence that 3% saline is better than Mannitol or vice versa.
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Mannitol's diuretic effect can lead to difficult-to-control diuresis and potential hypotension.
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Mannitol's first effect within 15 to 20 minutes is changing blood vessel rheology to allow freer passage through cerebral circulation and improve oxygen delivery, not diuresis.
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It's also important to remember that Mannitol does not work by diuresis effect first. It's actual first effect, which is within the first, 15 to 20 minutes of providing it is, it changes the rheology of the blood vessels.
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Steroids are no longer considered effective therapy for suspected spinal cord injury and may cause detriment.
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Even for those with suspected spinal cord injury, it is, that is no longer considered, uh, um, um, Actually effective therapy and it actually may cause detriment.
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Neurosurgical options after failed conservative treatment include simple evacuation of surgical lesions like epidurals.
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Decompressive craniectomy is an emerging option for diffuse axonal injury with difficult-to-control ICP when there is no true surgical lesion to decompress.
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In decompressive craniectomy, the bone is preserved and can be replaced after things settle down.
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For persistently elevated ICP above 20 with higher spikes, the patient will slowly deteriorate to the point of being unsalvageable without intervention.
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If you're persistently measuring ICPs above 20 and having, uh, higher spikes, you know that that patient is going to slowly deteriorate to the point where they're not going to be salvageable.
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Based on the third iteration of Management of Traumatic Brain Injury in Children published in Pediatric Critical Care Medicine, there is no clear consensus that decompressive craniectomy improves outcomes.
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At the present time, uh, based on the most recent publication of the guidelines, this is the 3rd iteration of the Management of traumatic brain injury in Children that was published in Pediatric Critical Care Medicine. There's still no, uh, clear consensus that decompressive craniectomy does, uh, improve the outcome of these patients
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Major trauma centers across North America are using decompressive craniectomy more frequently for severe TBI.
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CT scan is preferred in acute situations with acute ICP presentation because it provides the best information for determining need for OR or drain placement.
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I use the MRI more for, after the 1st 48 hours, once the patient is a bit more stable, once I've been able to control ICP spikes, and I use that more as a prognosticator.
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MRI is used after the first 48 hours once the patient is stable and ICP spikes are controlled, primarily as a prognosticator.
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MRI is useful in severe cases for counseling families and directing care plans, and can be repeated in a week to determine true extent of injury and level of disability.
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CT head scan can be completed in 5 minutes versus 20-30 minutes for MRI, making it preferable for critical patients.
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Sympathetic storming occurs due to imbalance of sympathetic and parasympathetic nervous systems as a result of head injury.
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Untreated sympathetic storming can lead to secondary brain injury or potentiate ongoing injury.
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Hyperventilation during sympathetic storming leads to vasoconstriction which could cause cerebral hypoxia and further cellular injury.
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Arrhythmias during sympathetic storming can lead to hemodynamic instability and hypoperfusion.
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Neurogenic pulmonary edema is sometimes common in TBI patients and can cause hypoxia and difficult ventilation.
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The cornerstone of sympathetic storming treatment is sedation and pain control, usually with narcotics and/or benzodiazepines as first-line medications.
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The cornerstone to treatment is sedation and pain control. This is usually accomplished with narcotics and or benzodiazepines as are your first line medications.
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Bromocriptine acts on the hypothalamus to reduce hyperthermia, diaphoresis, and blood pressure in sympathetic storming.
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Clonidine is an alpha-2 agonist that can reduce levels of catecholamines throughout the body and reduce ongoing sympathetic storm.
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Propranolol can help control arrhythmias and lower blood pressure in sympathetic storming.
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Oxycodone has been used for its longer-acting effect for pain control in sympathetic storming.
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